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26 Cards in this Set

  • Front
  • Back
What is the "fed" state?
--During and immediately after a meal
--Use nutrients to provide energy
--Store the extra energy as fuel stores.
When you eat something, what happens to the different components?
--Dietary Carbs-->monosaccharides-->GLUCOSE
--Dietary Protein-->AMINO ACIDS
--Dietary Lipid (Fat)-->CHYLOMICRONS
What happens in liver during fed state?
FED STATE-->Liver DIGESTS glucose.

--either OXIDIZE glucose or convert it to GLYCOGEN and TRIACYLGLYCEROLS

GLUCOSE-->pyruvate-->acetyl Coa-->TCA-->ETC-->ATP!

--Glycogen synthesis

GLUCOSE-->pyruvate-->FA + glycerol (lipogenesis)-->TRIACYLGLYCEROLS-->leave liver as VLDL's

A.ACIDS-->proteins (translation)
What happens in brain during fed state?
GLUCOSE-->pyruvate-->acetyl Coa-->TCA-->ETC-->ATP

-->glucose is only fuel that crosses blood/brain barrier!
What happens in RBC during fed state?

-Have ABSOLUTE dependence on glucose, because they LACK mitochondria (can't do pyruvate oxidation, TCA, oxidative phosphorylation)--only energy from glucose)
What is CORI cycle?
Lactate generated from anaerobic glycolysis in RBC is carried back to liver-->converted into pyruvate

--pyruvate can either: enter TCA cycle (if liver needs energy) or be stored as glycogen (if liver doesn't need energy)
What happens in muscle during fed state?
GLUCOSE-->pyruvate-->LACTATE or ATP
(both oxidative and anaerobic processes)

--Glycogen synthesis
Extra GLUCOSE-->glycogen
What happens to fats in liver during the fed state?
--De novo lipogenesis
GLUCOSE-->converted to FA's + Glycerol-->Triacylglycerol (TAG)-->VLDL's-->released into blood-->stored in adipose cells OR broken down by muscle for energy
What happens to fats in muscle and adipose cells during fed state?
TAGs are in Chylomicrons (comes from dietary fat) AND VLDL's (made from lipogenesis in liver)

--Chylomicrons travel to tissue-->TAG's are broken down into glycerol and FFA
--VLDL's are transported to muscle or adipose tissue and serve similar purpose as chylomicron TAGs.

--FFA are collected-->TAGs reformed.
--ALSO adipose tissue can convert glucose-->TAGS by de novo lipogenesis.

--FFA-->Acetyl Coa (Beta oxidation)-->TCA-->oxidative phosphorylation.
BIG picture--what are the major metabolic events in fed state?
1) LIVER uses GLUCOSE and AMINO ACIDS for energy needs and conversion into glycogen, fat, protein (glycolysis, glycogen synthesis, de novo lipogenesis, translation)

2) BRAIN oxidizes GLUCOSE to make energy (glycolysis)

3) RBC's convert GLUCOSE-->LACTATE (anaerobic glycolysis-->CORI cycle)

4) MUSCLE converts GLUCOSE to LACTATE (anaerobic glycolysis) or CO2 (glycolysis). Converts FFA into CO2 (B-oxidation). Extra glucose-->glycogen (glycogenolysis)

5) ADIPOSE stores TAG.
What is the "fasted" state?
--Few hours after a meal.
--Have used up all the dietary nutrients for energy OR stored them.
--Now, you need to use STORES to meet ENERGY NEEDS.
--Most importantly--need to provide GLUCOSE to the BRAIN and RBC, because it's all they have.
What hormones initiate "fasting" state?
--Decreased insulin secretion, increased glucagon secretion!
What happens in liver during fasting state?
FASTING STATE-->Liver PRODUCES glucose for the rest of the body

--Glycogen stores-->GLUCOSE-->RELEASED to BRAIN and RBC's

--CORI cycle returns LACTATE to liver from RBC-->converted to GLUCOSE-->RELEASED to BRAIN, RBC's.

Beta Oxidation
FFA-->Acetyl Coa-->TCA-->oxidative phosphorylation (ETC)-->ATP!
(Eventually, KETOGENESIS occurs. Acetyl Coa-->KB's)
What happens in muscle during fasting state?
--Muscle protein broken down (proteolysis)-->releases alanine-->goes to liver (alanine cycle)-->converted to GLUCOSE (gluconeogenesis)

--Proteolysis also releases glutamine-->supports nucleotide synthesis in dividing tissues-->creates alanine-->goes to liver-->converted to GLUCOSE (gluconeogenesis)

Beta oxidation
FFA-->Acetyl Coa-->TCA-->oxidative phosphorylation (ETC)-->ATP!
What happens in adipose tissue during fasting state?

FFA-->used in beta oxidation

GLYCEROL-->used in liver for gluconeogenesis.
What is ketogenesis?
--During long fast, too much acetyl Coa is made by beta-oxidation-->can no longer enter TCA cycle.
--excess acetyl Coa-->ketone bodies!
-->can generate energy in brain and muscle-->spares glucose for RBC, which NEEDS it.
How are delta-G and delta-G* computed?

How do they affect whether biochemical reactions occur?
delta G=delta-G*+RTln[products]/[reactants]

--delta-G* is a CONSTANT-->measure of INHERENT ability of reactants to make products. (Keq is measured in test tube w/fixed amount of products, reactants-->rxn allowed to go to completion, then determine rxn specifics
-->if Keq>1, delta-G* is negative-->makes delta-G negative-->exergonic!
-->if Keq=<1, delta-G* is positive-->makes delta-G positive-->endergonic!
If a reaction is energetically unfavorable, how can you get it to occur?
--Need your delta-G to be negative
--Overall, reactions are additive-->so..can couple reactions w/ATP hydrolysis to make an OVERALL negative delta-G*-->makes a negative delta-G-->spontaneous rxn
-->can also use substrate level phosphorylation to make ATP. High energy phosphate bond on another molecule is cleaved, releasing energy, which drives endergonic formation of ATP.
What are roles of NAD, NADP, FAD, and CoA in metabolism?
-->electrons/protons are removed and transferred to NAD+, NADP+, FAD+-->forms NADH, NADPH, FADH-

NADH/FADH--> dump their electrons/protons into ETC-->make ATP!

NADPH-->gives up electrons/protons to produce reducing equivalents to make macromolecules and neutralize oxygen species.

CoA-->another important carrier in metabolism.
-->Acetic and fatty acids not v. reactive-->bound to CoA->forms acetyl CoA and acyl CoA-->SUPER reactive!
What are ways that metabolic pathways are regulated?
1) reversible phosphorylatio-->add (kinase) or remove (phosphatase) to/from serine, threonine, or tyrosine-->can ACTIVATE or INACTIVATE enzyme.

2) allosteric regulation-->small molecules bind to enzyme-->alter activity
3) change enzyme level-->signals will increase synthesis of enzymes when they need them in pathways (induction) or turn off production if they're not needed (repression)
4) compartmentalization-->pathways can use COMMON intermediates-->keep these substrates separate (different compartments) to decrease competition for intermediates.
What is glycolysis?
glucose-->pyruvate (aerobic)
glucose-->lactate (anaerobic)

pyruvate-->fat (lipogenesis)
pyruvate-->acetyl Coa-->TCA-->oxidative phosphorylation (oxidation)
What is lipolysis?
hydrolysis of stored TAGs-->FFA+glycerol-->transported to tissues for energy generation
What is glycogenolysis?
What is beta-oxidation?
oxidation of FFA-->produces acetyl CoA in the mitochondria
What is proteolysis?
Breakdown of proteins into a.acids-->used in gluconeogenesis
What is ketogenesis?
Acetyl Coa-->ketone bodies